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Merck

K1005

Sigma-Aldrich

Monoclonal Anti-Kinesin antibody produced in mouse

clone IBII, ascites fluid

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About This Item

MDL number:
UNSPSC Code:
12352203

biological source

mouse

conjugate

unconjugated

antibody form

ascites fluid

antibody product type

primary antibodies

clone

IBII, monoclonal

mol wt

antigen 40-80 kDa (Two bands. Additional bands at 130-140 kDa may be present.)

contains

15 mM sodium azide

species reactivity

rat, sea urchin, frog, bovine

technique(s)

western blot: 1:500 using kinesin-enriched rat brain preparation

isotype

IgM

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

Gene Information

Specificity

The antibody recognizes the kinesin heavy chain.

Immunogen

kinesin from bovine brain.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class

12 - Non Combustible Liquids

wgk_germany

nwg

flash_point_f

Not applicable

flash_point_c

Not applicable


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Greta Forlani et al.
The FEBS journal, 273(10), 2127-2138 (2006-05-03)
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In the central nervous system (CNS), three types of myelin-associated inhibitors (MAIs) have major inhibitory effects on nerve regeneration. They include Nogo-A, myelin-associated glycoprotein, and oligodendrocyte-myelin glycoprotein. MAIs possess two co-receptors, Nogo receptor (NgR) and paired immunoglobulin-like receptor B (PirB).
Rollin W Robinson et al.
Histochemistry and cell biology, 122(1), 1-5 (2004-06-09)
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G Amadoro et al.
Neurobiology of aging, 32(6), 969-990 (2009-07-25)
Alzheimer's disease (AD) is characterized by Aβ overproduction and tau hyperphosphorylation. We report that an early, transient and site-specific AD-like tau hyperphosphorylation at Ser262 and Thr231 epitopes is temporally and causally related with an activation of the endogenous amyloidogenic pathway

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